オオニシ ジュンジ  onishi junji
大西 淳之

  • 所属   東京家政大学  家政学部 栄養学科
  •     東京家政大学大学院  人間生活学総合研究科 健康栄養学専攻
  •     東京家政大学大学院  人間生活学総合研究科 人間生活学専攻
  •     東京家政大学短期大学部  短期大学部 栄養科
  • 職種   教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 Alteraions of angiotensin II receptor contents in hypertrophied hearts.
掲載誌名 正式名:Biochemical and Biophysical Research Communications
略  称:Biochem Biophys Res Commun
ISSNコード:0006291X/10902104
掲載区分国外
巻・号・頁 212(2),pp.326-333
著者・共著者 ◎Fujii N, Tanaka M, Ohnishi J, Yukawa K, Takimoto E, Shimada S, Naruse M, Sugiyama F, Yagami K, Murakami K,
発行年月 1995/07
概要 Tsukuba hypertensive mice, which carry the human genes for renin and angiotensinogen, show cardiac hypertrophy as well as hypertension due to activation of the renin-angiotensin system (RAS). Here, we compared the cardiac angiotensin II (Ang II) receptor contents in these and normotensive control mice by means of ligand binding studies and competitive reverse transcription-polymerase chain reaction analyses. The content of the Ang II receptor type 1 (AT1) was significantly higher at both the protein (2.5-fold; p < 0.01) and mRNA (1.4-fold; p < 0.05) levels in the hypertensive mice than that in control mice. Almost identical levels of the Ang II receptor type 2 (AT2) expression were identified at the mRNA levels in the two types of mice, although the levels were less than 20% of those of AT1 mRNA in control mice. These results suggest that AT1 in the heart is upregulated in response to Ang II-induced hypertrophic change and that, in particular, the upregulation of AT1 in particular contributes to the development and/or maintenance of cardiac hypertrophy in conjunction with the increase in Ang II production, because AT1 is responsible for cardiac hypertrophy related to the RAS.
DOI doi:10.1006/bbrc.1995.1973
PMID PMID: 7542873